Glutamate receptors and their associated ion channels are responsible for most of excitatory transmission in the central nervous system. Certain types of glutamate receptors, whose activation is crucial in experimental models of learning and memory, have been implicated in such processes as epilepsy, ischemic neuronal injury and neurodegenerative diseases such as Alzheimer's dementia. By studying glutamate receptors at the single channel/receptor level it is possible to determine how their properties are modified in the rodent in vitro brain slice preparation as it is used for studying long-term potentiation (LTP), an experimental model of learning and memory. Recent work has indicated that the functional properties of these receptors can be altered by phosphorylation and that the expression of LTP can be altered by agents which alter phosphorylation. Therefore, it has been proposed that one of the mechanisms for the expression of LTP involves phosphorylation of these receptors, however the direct connection between LTP, phosphorylation of glutamate receptors and an alteration of glutamate receptor function has only been inferred. This connection can be made by using patch-clamp techniques to study the properties of individual glutamate receptors removed from the synaptic regions of dendrites before and after manipulations which induce LTP and in the presence of drugs which interfere with phosphorylation of these receptors. Illucidation of this connection and the resulting changes in glutamate receptors as might be altered by pharmacological agents could provide insight into therapeutic solutions for the disease processes mentioned above.